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1. IMMUNOLOGY > lecture 8 > Flashcards

lecture 8 Flashcards

1
Q

when is the stimulation of the immune response is harmful

A

The immune response is there to protect against a variety of invading pathogens

Sometimes adaptive immune responses are generated against harmless antigens which are not associated with a disease causing organism

These reactions are known as hypersensitivites or more generally as allergic reactions

Immune disorders have a genetic and environmental component

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2
Q

what are the 4 major types of allergic reactions

A

There are 4 major types of allergic reactions classified according to the immune reactant

TABLE IN L8 S4

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3
Q

Type 1 Hypersensitivity

A

Type 1 allergies are caused by sensitisation of an individual to an innocuous antigen by the production of an IgE response

Subsequent exposure to the allergen triggers the activation of IgE bearing cells like mast cells and basophils

Some individuals have a predisposition to develop allergic reactions known as ATOPY

The development of atopy has both genetic and environmental components

The major normal role of IgE is in clearance of worm infections

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4
Q

Environmental factors in allergy

A

Atopic allergic disease is on the increase worldwide

  • This corresponds with the reduced exposure in children to infectious disease
  • Changes in exposure to animal and soil micro-organisms
  • Changes in the intestinal microbiota

Lead to the formulation of the hygiene hypothesis- now modified as the counter-regulation hypothesis

  • Proposes that immune stimulation in general protects against atopy
  • This produces IL-10 and TGFβ which down regulates TH1 and 2 cells
  • Decreased microbial stimulation also in some way reduces the production of Treg cells
  • Treg can control allergy by suppressing TH2 cytokine production
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5
Q

what do the symptoms of allergic reactions depend on?

A

The symptoms of allergic reactions depend on the site of mast cell degranulation

TABLE IN L8 S7

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6
Q

process of the Sensitisation to the house dust mite allergen Der p1

A

Class switching to IgE production is directed by the cytokine IL-4 produced by TH2 cells

  • the enzyme Der p 1 cleaves occludin in tight junctions and enters mucosa
  • dendritic cell prime cell in lymp node
  • plasma cell travels back to mucosa and produces Der p 1- specific IgE antibodies
  • Der p 1-specific IgE binds to mass cell, Der p 1 triggers mast-cell degranulation
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7
Q

what happens when antigen binds to IgE

A

Antigen binding to IgE leads to the amplification of IgE production

  • IgE secreted by plasma cells binds to a high affinity Fc receptor FceRI on mast cells
  • activated mast cells provide contact and secreted signals to B cells to stimulate IgE production
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8
Q

features of airborne allergens that may promote the priming of Th2 cells that drive IgE responses

A
  • protein, often with carbohydrate side chains
  • low dose
  • low molecular weight
  • highly soluble
  • stable
  • contains peptides that bind host MHC class II
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9
Q

Mast cell activation has different effects on different tissues

A

effects on gastrointestinal tract, on eyes / nasal passages / airways and on blood vessels

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10
Q

define anaphylaxis

A

If antigen is injected straight into the blood stream then anaphylaxis can result as connective tissue mast cells throughout the body become activated.

Mild activation can result in urticaria.

Severe activation can result in anaphylactic shock, resulting in catastrophic loss of blood pressure due to increased vascular permeability and death.

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11
Q

risk factors for the development of food allergy

A

Food allergy is relatively common and can give systemic and gut effects

  • immature mucosal immune system
  • early introduction of solid food
  • hereditary increase in mucosal permeability
  • IgA deficiency or delayed IgA production
  • inadequate challenge of the intestinal immune system by commensal flora
  • genetically determined bias toward a Th2 environment
  • polymorphisms of Th2 cytokine or IgE receptor genes
  • impaired enteric nervous system
  • immune alteration like low levels of TGFB
  • gastrointestinal infections
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12
Q

treatments for allergic diseases

A
  • mediator action
  • chronic inflammatory reactions
  • Th2 response
  • IgE binding to mast cells

TABLE IN L8 S14

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13
Q

Non-IgE mediated allergic disease

A

Type II Antibody-mediated hypersensitivity reactions
- Can be caused by some drugs-eg penicillin. The drug binds to the cell surface of RBCs and induces an antibody response. Clearance of cells by FcR bearing macrophages causes anaemia

Type III Complex-mediated hypersensitivity reactions
- Arise following stimulation with soluble antigens and cause an immune complex disease. Deposition of immune complexes is very harmful- disease depends where this happens. Eg serum sickness

Type IV Delayed-type hypersensitivity reactions
- These are mediated by antigen specific effector T cells of TH1 or CD8+ subtypes. Release of cytokines from the activated cells causes the problems. Eg coeliac disease

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14
Q

Harmful cytokine production following Th1 antigen stimulation

A

DIAGRAM IN L8 S16

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15
Q

Coeliac disease a Type IV hypersensitivity

A

Caused by an immune response to the food allergen gluten.

Causes a pathology in gut where:

  • the intestinal villi are lost
  • severe inflammation of the intestine wall occurs
  • increase in number of intestinal lymphocytes occurs

Has a strong genetic element being associated with HLA DQ2 which has an unusual binding groove, binding peptides with glutamic acid.
- Such a peptide can be generated by the transamination of gliadin, a component of gluten

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16
Q

Molecular basis of immune response to gluten

A

DIAGRAM IN L8 S18-19

17
Q

autoimmunity

A

The response to self antigens is called autoimmunity and can lead to very damaging autoimmune disease

Normally the repertoire of antigen specific receptors generated at random by recombination is ‘screened’ for self reactivity and any self reactive cells inactivated- self tolerance

Autoimmunity results when those processes of self tolerance break down

18
Q

review of mechanisms of self tolerance

A

Cells which recognise a self peptide receive a negative signal leading to death or inactivation- central tolerance.

High, sustained levels of expression of an antigen usually correlate with self and lead to tolerised lymphocytes in this case the receptors have been strongly and constantly engaged.

Innate immune signals like proinflammatory cytokines signal infections and provide co stimulatory signals. In their absence T cells can become Treg or receive a negative interacting signal- peripheral tolerance.

So a variety of different mechanisms sequential mechanisms act as checkpoints to generate self tolerance and normally prevent autoimmunity.

19
Q

Some common autoimmune disorders

A
  • psoriasis
  • rheumatoid arthritis
  • graves disease
  • hasimotos thyroiditis
  • systemic lupus erythematosus
  • sjorgen syndrome
  • crohn’s disease
  • multiple sclerosis
  • type 1 diabetes (insulin dependent diabetes mellitus IDDM)
20
Q

Autoimmune diseases can be divided into organ-specific and systemic

A

organ-specific autoimmune diseases:

  • type 1 diabetes mellitus
  • goodpasture’s syndrome
  • multiple sclerosis chron’s disease psoriasis
  • grave’s disease

systemic autoimmune diseases:

  • rheumatoid arthritis
  • scleroderma
  • systemic lipid erythematosus
21
Q

requirements for the development of autoimmunity

A

genetic factors
infection and environmental exposure
immune regulation
autoimmunity

22
Q

Association of MHC alleles with disease susceptibility illustrates a genetic component

A

so…?

23
Q

Other genetic evidence….

A

Defects in cytokine signalling or production

  • Overexpression eg TNFα in RA
  • Underexpression eg IL-10 in IBD

Mutations in genes involved in one or more normal immune mechanisms of tolerance

  • Antigen clearance eg C1q KO causes Lupus
  • Treg development eg Foxp3 KO causes multi organ autoimmunity

Mutations in single genes – these are very rare

24
Q

Infection can be an environmental trigger to develop autoimmunity by breaking self-tolerance

A

disruption of cell or tissue barrier
will release the sequestered self antigen and activate nontolerized cells
(eg sympathetic opthalmia)

molecular mimicry
production of cross reactive antibodies or T cells
( eg rheumatic fever, reactive arthritis or lyme arthritis)

25
Q

Release of sequestered antigens can lead to autoimmunity - mechanism

A

trauma to one eye results in the release of sequestered intraocular protein antigens

released intraocular antigen is carried to lymph nodes and activates T cells

effector T cells return via bloodstream and encounter antigen in both eyes

26
Q

Type II autoimmune diseases

A

TABLE IN L8 S29

27
Q

Some Type II autoimmune diseases are directed against cell surface receptors

A

TABLE IN L8 S30

28
Q

Graves disease leads to hyperthyroidism - mechanism

A

DIAGRAM IN L8 S31

29
Q

Myasthenia Gravis leads to progressive muscle paralysis

A

DIAGRAM IN L8 S32

30
Q

Type III autoimmune diseases

A
  • mixed essential cryoglobulinemia

- rheumatoid arthritis

31
Q

Type IV autoimmune diseases

A 
type 1 diabetes
rheumatoid arthritis
multiple sclerosis
crohn's disease
psoriasis
32
Q

why are some alleles susceptible

A

Susceptible alleles have a particular binding groove

DIAGRAMS IN L8 S36

1. IMMUNOLOGY (7 decks)

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